Diabetes and endocrinology Flashcards
1
Q
Describe the thyroid gland anatomically and explain the way it moves
A
A L lobe and a R love joined together by an isthmus. Sits anterior to the thyroid cartilage within the neck. Moves on swallowing as thyroid cartilage moves on swallowing.
2
Q
What remnant tissues can be left from the embryological migration of the thyroid?
A
- Thyroglossal cyst
- Lingual thyroid
3
Q
What structures can be damaged in thyroid surgery?
A
Recurrent laryngeal nerve - lies laterally on either side of the thyroid
Parathyroid gland - lies anteriorly
4
Q
What is the blood supply of the thyroid?
A
Sup and inf thyroid arteries
5
Q
How does the thyroid synthesise hormones and where does it store them?
A
Follicular cells secrete thyroglobulin - > thyroxine (T4) which is stored in colloid tissue.
C cells secrete calcitonin.
6
Q
What is the difference between T3 and T4?
A
T4 in main circulation and is converted peripherally to short acting T3.
7
Q
What are the actions of T3 and T4?
A
- Increase BMR
- Growth in childhood
- Increase HR and increase peripheral vasodilation near the body’s surface
- Increase myelination of nerves
8
Q
What is the TFT of primary hypothyroidism?
A
Increased TSH and decreased T4.
Problem w the thyroid gland, often autoimmune.
9
Q
What is the TFT of secondary hypothyroidism?
A
Decreased T4 and non elevated TSH.
Normally TSH def caused by pituitary disease.
10
Q
What is the TFT of hyperthyroidism?
A
Increased T4 and T3, reduced TSH.
11
Q
What factors affect TFTs?
A
- Pregnancy
- Lithium
- Amiodarone
12
Q
What are the causes of hyperthyroidism?
A
- Grave’s
- Nodular thyroid disease
- Thyroiditis
13
Q
What is Grave’s?
A
Autoimmune TSH receptors stim Ab. Relapsing and remitting disease, most common in young women.
14
Q
What is nodular thyroid disease?
A
Excess secretion of T3+T4 from nodules within a toxic multi nodular goitre. More common in elderly people.
15
Q
What is thyroiditis?
A
Inflam of the thyroid causes release of thyroxine. Caused by viral infection, childbirth and meds eg. amiodarone.
16
Q
What are the clinical features of hyperthyroidism?
A
Caused by increased sympathetic activity: - Weight loss w increased appetitie - Insomnia, irritability, anxiety - Heat intolerance due to increased BMR - Palpitations and tremor Extra sx: - Pruritis - Diarrhoea - Reduced fertility and menstrual irregularity
17
Q
What are the presentations of hyperthyroidism in children and the elderly?
A
Children - accelerated growth and behavioural defects
Elderly pt - reduced energy levels
18
Q
What are the signs of hyperthyroidism?
A
- Tachycardia
- Warm peripheries
- Tremor
- Hyper reflexia and lid lag
19
Q
What causes lid lag?
A
Increase sympathetic activity in the upper eyelid. Superior tarsal muscle is supplied by sympathetics and aids levator palpebris superioris (oculomotor nerve) to elevate eye.
20
Q
What are the specific signs of Grave’s disease?
A
- Thyroid eye disease = lid retraction and proptosis
- Pretibial myxoedema = red and swollen shins
- Thyroid acropachy = clubbing
21
Q
What are the hyperthyroidism TFTs?
A
- Elevated T3 and T4 w nondetectable TSH
- Subclinical hyperthyroidism = normal T3/T4 and reduced TSH
22
Q
What are the other Ix into hyperthyroidism?
A
- Thyroid USS - can confirm if nodular thyroid disease but doesn’t measure thyroid activity
- Nuclear imaging - detects cause of hyperthyroidism
- Thyroid peroxidase Ab (TPO) is non specific marker for autoimmune disease, TSH receptor stim Ab is more specific
23
Q
What are the medical treatments of hyperthyroidism?
A
Thionamides eg. carbamizole reduce the synthesis of T3/T4. They normally take 4-6 weeks to normalise TFTs and in the mean time a B blocker can be used to control sx.
If sore throat - need FBC, may have bone marrow suppression.
24
Q
What are the SE of thionamides?
A
- Generalised rash
- Bone marrow suppression - if unexplained fever or sore throat do FBC to see if pancytopenia - stop meds if neutropenia
25
What are the definitive treatments of hyperthyroidism?
- Radioactive iodine
| - Thyroidectomy
26
Describe using radioactive iodine as a treatment of hyperthyroidism
One single dose of 131 iodine.
Don't use in pregnant women and don't get close to pregnant women or children a few days after as pt becomes radioactive.
Can worsen thyroid eye disease and often causes hypothyroidism so pt will need life long thyroxine supplement.
27
What are the complications of a thyroidectomy?
- RLN palsy as anatomically close
- Hypocalcaemia due to hypoparathyroidism
- Bleed, infection
28
What are the primary causes of hypothyroidism?
- Autoimmune disease eg. Hashimoto's
- Drugs eg. amiodarone + lithium
- Genetic defect reducing T3/T4 synthesis
- Iodine def can cause in neonates and causes 'cretinism'
- Transient or perm after pregnancy + can be mis diagnosed as post natal depression
- Iatrogenic - treatment for hyperthyroidism or radiation to neck
29
What are the secondary causes of hypothyroidism?
Less common than primary causes. TSH def due to hypothalamic pit disease = reduced T4 and non elevated TSH.
30
What are the clinical features of hypothyroidism?
```
Sx similar to depression/chronic fatigue:
- Weight gain
- Cold intolerance
- Fatigue
- Bradycardia
- Constipation
- Myxoedema around eyes
Most commonly an incidental finding.
```
31
What is Hashimoto's thyroiditis?
Enlarged thyroid gland with hypothyroidism
32
What are the Ix into hypothyroidism?
- TFT = reduced T4 and increased TSH (increased TSH enough to diagnose primary but need T4 to diagnose secondary)
- Thyroid Ab to confirm autoimmune disease, TPO strongly positive in Hashimoto's
33
What is the treatment of hypothyroidism? What are the problems of replacement?
- Thyroxine replacement - 50-100 ug/day
- Increased TSH = under replacement, non compliance of malabsorption
- Reduced TSH = over replacement, increases risk of Afib and osteoporosis
34
What is subclinical hypothyroidism?
- Normal T4 and increased TSH
| - In this case asymptomatic pt doesn't need treatment and thyroid func often spontaneously resolves
35
When should treatment be offered in subclinical hypothyroidism?
- Symptomatic
- Pregnant or planning
- Dyslipidaemia
- If +ve thyroid Ab annual TFTs to ensure don't develop overt hypothyroidism
36
What are the parts of the adrenal gland?
Adrenal gland sits on top of the kidney and is made up of the adrenal medulla (centrally) and the adrenal cortex (on the outside).
37
What does the adrenal cortex secrete?
GAM:
- Glucocorticoids
- Adrenal androgens
- Mineralcorticoids
38
What do glucocorticoids do? What hormone controls their release?
Cortisol is the main one and it has a role in metabolism, controlled by ACTH. -ve feedback on the hypothalamus to reduce CRH, ACTH and ADH.
Highest in the morning and lowest at night.
Is only biologically active when free but most in blood is bound.
39
What do adrenal androgens do?
Have a role in puberty and adult females, (male androgens from testes).
Act on the sebaceous glands, hair follicles, ex genitalia and prostate.
40
What do mineralcorticoids do?
Aldosterone is the main one, controlled by RAAS and stim by Ang2.
Acts on the DCT to increase Na retention and reduce K+ excretion.
41
What is the adrenal medulla?
Is made up of sympathetic NS and secretes adrenaline, noradrenaline and dopamine.
42
What is Addison's and what causes it?
Primary adrenal insufficiency.
| Causes - destruction of the adrenal gland or genetic defect in steroid synthesis. All 3 adrenal cortex affected.
43
What are the clinical features of Addison's and why do pt get them?
- Fatigue, weakness, anorexia, weight loss, nausea, abdo pain
- Postural hypertension (reduced mineralcorticoids)
- Hypoglycaemia (reduced glucocorticoids)
- Increased pigmentation (increased ACTH as no neg feedback)
44
What are the Ix into Addison's?
- Low 9am cortisol
| - Primary adrenal failure normally shows = low Na, high K, increased urea, hypoglycaemia and anaemia
45
What is the management of Addison's?
Life long replacement of gluticorticoids = hydrocortisone or low dose prednisolone and mineralcorticoids = fludrocortisone.
Pt need to double G dose during illness and need to take IV in surgery, diarrhoea or vom.
46
What is an Addisonian crisis? How is it treated?
```
Features = collapse, coma, dehydration, hypotension, increased pigmentation.
Treat = IV fluids and hydrocortisone.
```
47
What is the cause of secondary adrenal insufficiency?
ACTH deficiency - can be caused by long term steroid use which suppresses ACTH. Sudden stopping of steroids can cause an adrenal crisis.
48
What are the disorders of the adrenal medulla?
- Phaeochromocytoma
| - Paraganglioma
49
What are phaeochromocytomas and paragangliomas?
Tumours that release excess catecholamines.
| Phaeochromocytoma stems from the adrenal medulla but a paraganglioma stems from extra adrenal chromaffin tissue.
50
When are disorders of the adrenal medulla suspected to have a familial link?
- When a pt presents at a young age
- When the tumour is bilateral, malignant or extra adrenal
Will need to do genetic testing to confirm.
51
What are the clinical features of paheochromocytomas and paragangliomas?
- Sweating
- Palpitations, anxiety, panic attacks
- Headaches
- 90% have HTN
- If untreated = hypertensive crisis
52
What are the clinical features of a hypertensive crisis?
Huge HTN with organ damage - encephalopathy, pulm oedema, hyperglycaemia, cardiac arrhythmia. Can cause death.
53
What are the Ix into phaeochromocytomas and paragangliomas?
- 24 hr catecholamine and plasma metanephrine (will be elevated)
- CT/MRI to localise tumour, abdo normally but can do full body
54
What is the definitive management of phaechromocytomas and paragangliomas?
Surgical excision, either lapro or open = removal of one or both of the adrenal glands.
55
What is the medical management of phaechromocytomas and paragangliomas? What order do you do it in?
All pt diagnosed with either need to be on a/B blockade.
a = phenoxybenzamine or doxazosin. Do a first to avoid a adrenergic stim which could cause HTN crisis. Add B blocker to control tachycardia if needed.
56
Draw the anatomy of the pituitary gland and label nearby structures
Answers on iPad
57
What is within the cavernous sinus?
```
Cranial nerves:
- 3 = oculomotor
- 4 = trochlear
- 6 = abducens
- Va and b branches of trigeminal (5)
and the int carotid artery.
```
58
What are the 5 pituitary axes?
1. Growth axis
2. Thyroid axis
3. Gonadal axis
4. Prolactin axis
5. Adrenal axis
59
Describe the growth axis and the hormones job
Growth hormone - growth in children and maintaining healthy muscle in adults. At the liver produces IGF-1 which is a marker for GH.
+ve control = GHRH
-ve control = somatostatin
60
Describe the thyroid axis and the hormones jobs
TSH released and acts on thyroid to release thyroxine.
+ve control = TRH
-ve control = thyroxine
61
Describe the gonadal axis and the hormones jobs
LH = ovulation and corpus luteum in women, testosterone from Leydig cells in men.
FSH = ovarian follicle in women, sperm synthesis in men.
+ve control = GnRH
-ve control = testosterone and oestrogen
Prolactin directly inhibits LH and FSH.
62
Describe the prolactin axis and the hormones jobs
Prolactin causes lactation and directly inhibits LH and FSH.
+ve control - TRH a bit
-ve control - dopamine, anything that blocks dopamine increases prolactin
63
Describe the adrenal axis and the hormones jobs
ACTH high in the morning and low at night, causes cortisol release.
+ve control - CRH
-ve control - cortisol
64
What are the clinical sign of pathology of the pituitary gland?
Pit tumours present due to compression of adjacent structures or excess of hormones:
- Compression of optic chiasm = bi temporal hemianopia
- Hormone excess = Cushing's, acromegaly, hyperprolactinoma, hypopituitism
65
What is the indication for surgery on the pit gland?
Optic chiasm compression causing bi temporal hemianopia
66
What are the basal biochem tests for assessing the pit gland?
- IGF-1 is the marker for GH
- FSH + LH should be measured in a womens first 5 days of menstrual cycle and at 9am for men
- Cortisol at 9am
- Prolactin and TSH can check at any time of day
67
What are the dynamic bio chem tests?
- Insulin tolerance test
| - Synacthen test (synthetic ACTH)
68
What is the synacthen test?
When there has been ACTH def for 2 weeks+ there is atrophy of the adrenal cortex and it will no longer be stim to make cortisol by the synacthen.
69
What is the insulin tolerance test?
If you get hyperglycaemia with symptoms GH and ACTH will increase - not sure I understand this.
70
What imaging is used in the assessment of the pit gland?
MRI w contrast - should be able to differentiate between the tumour and the gland.
>1 cm = macro
<1 cm = micro
71
What are the alternative causes of hyperprolactinaemia (not prolactinoma)?
- Pregnancy
- PCOS
- Profound hypothyroidism but is rare
- Dopamine antagonists eg. anti emetics and anti psychotics
72
What are the demographics and presentation of a microprolactinoma? How does a macroprolactinoma differ?
Micro = women > men
Macro = men > women
Presentation - menstrual disruption, infertility, galactorrhoea, hypogonadism in men
73
How can you differentiate between PCOS and microprolactinoma?
In PCOS there is androgenic sx, PRL is normally <1000 iU/L and there is no pit lesion found on MRI.
74
What level of prolactin suggests an active prolactin secretion?
>5000 iU/L
75
What is the treatment of hyperprolactinaemia?
Dopamine agonists - cabergoline (1/2 times a week so better tolerated) or bromocriptine (every day).
76
What are the side effects of dopamine agonists to treat hyperprolactinaemia?
- Nausea
- Postural hypertension
- Psych disturb
77
What are the causes of acromegaly?
GH secreting pit tumour
78
What is the appearance of a person with acromegaly?
- Increased size of hands and feet
- Prominent forehead and chin, gapped teeth
- Soft tissue inflam = large tongue and soft palate = sleep apnoea and swollen hands = carpal tunnel syndrome likely
79
What are the clinical features of acromegaly unrelated to appearance?
- Sweating
- Headaches
- HTN
- Diabetes mellitus
80
What are the risks of leaving acromegaly untreated?
- Facial deformities/disfiguring features
| - CVS disease and death
81
What are the ix into acromegaly?
- Oral glucose tolerance test
- Measure IGF-1 levels, elevated
- Pit MRI - will usually see pit tumour
82
What is a co secreting tumour in acromegaly?
Often the GH secreting pit tumour will also secrete prolactin, so will also have raised PRL
83
What is an OGTT?
Oral glucose tolerance test = measure GH before and then give pt a sugary drink, if GH isn't decreased pt has acromegaly.
Glucose should normally cause a decrease in GH.
84
What is the management of acromegaly?
- Surgical = remission more likely in microadenomas than macroadenomas
Medical:
- Stereotactic RT
- Somatostatin analogues by monthly injection
- GH receptor blockers
85
How do you monitor acromegaly?
- After surgery = measure GH to see if persistent disease
- Colonoscopy screening as acromegaly increases risk bowel cancer
- Screen for sleep apnoea, DM and CVS risk
86
What is a non functioning pit adenoma?
A biochemically inactive tumour but instead causes sx by compression = hypopituitarism, visual field loss and headache.
87
When is surgery on a NFPA indicated?
Causing visual field loss or a threat to vision
88
What are the causes of hypopituitarism?
- Acquired = pit tumour, inflam or infiltrative disease, traumatic brain injury, RT
- Congenital, present when young
89
What are the sx of hypopituitarism?
- Lethargy
- Weight gain
- Sexual dysfunction
- Short stature in children
90
What should you suspect in a pt w pit disease and a reduced QOL? What is the pt composition like?
Suspect GH def - reduced muscle and bone mass with increased fat
91
What are the ix into hypopituitarism?
- Reduced T4, non elevated TSH
- Reduced sex hormones, non elevated LH and FSH
- IGF-1 reduced
- Tumour on MRI
92
What is the treatment of hypopituitarism?
- ACTH def = hydrocortisone
- TSH def = throxine
- GH def = daily GH injections
- Sex hormone def = testosterone infections in men and O+P in women, COCP or HRT
93
What is needed to confirm a DKA diagnosis?
- BM >11 mmol/L or known DM
- Ketonuria >2 or blood ketones >3 mmol/L
- pH <7.3 or bicarb < 15 mmol/L
94
What is the immediate management of DKA?
- AtoE - RR, pulse oximetry, pulse, BP, temp, EWS, GCS
- Set up IV access
- Cap blood glucose and blood ketones
- Urinalysis for ketones
- Bloods - FBC, U&Es, blood ketones, bicarb
95
What actions do you take after the immediate management of DKA?
- IV fluid prescription - 0.9% NaCl
- 10 units insulin STAT, then continual fixed rate infusion
- K+ replacement = 20 mmol in 500 ml
- Glucose infusion to prevent hypoglycaemia, 5% dextrose
96
Give some detail for IV fluid prescribing in DKA
```
If systolic BP over 90mmHg:
1st = 1L NaCl 0.9% over 1 hour then..
- 1L over 2 hrs x2
- 1L over 4 hrs x2
- 1L over 6 hrs x2
If systolic BP under 90mmHg - NaCl 0.9% 500ml over 15 mins.
```
97
How do you monitor a pt w DKA?
- After 1 hour do cap blood glucose and U&Es
| - Cont pulse oximetry and cardiac monitoring if required
98
What are the indications of severe DKA?
- GCS <12
- Pulse >100 or <60 BPM
- BP <90mmHg systolic
- O2 sats <92%
- pH <7
- Hypokalaemia on admission
99
What are the signs and symptoms of DKA?
Sx - palpitations, sweat, thirst, weight loss, N+V, abdo pain
Signs - tachy, hypotension, reduced skin turgor, Kassmaull breathing, dry mucous membrane, reduced urine output and consciousness
100
What are the causes and RF of DKA?
- BM constistently >15 mmol/L
- Missing insulin injections or a fault w insulin pen
- Infection
- Excess alcohol consumption or illegal drug use
- Prolonged period of stress
101
What is HHS?
Hyperosmolar hyperglycaemic state. Occurs in T2DM and is a combination of dehyrdration and illness.
Skipping meds in illness or hormones in illness cause hyperglycaemia.
102
What is the triad of HHS?
1. Hyperglycaemia >30mmol/L
2. Absence of significant acidosis
3. High serum osmolality >320 mosmol/Kg
103
What are the sx of HHS?
- Thirst and dry mouth+skin
- Nausea
- Urination
- Alt consciousness
104
What is the management of HHS?
- Insulin at a fixed rate infusion
- Monitor K+ and replace when necessary
- IV fluid prescription according to protocol and w caution in elderly to avoid fluid overload
- LMWH for prophylaxis
- Find and treat underlying cause
105
What is the diagnostic criteria for T1DM?
- Symptoms + one abnormal result or two abnormal results on two different times
- Sx = weight loss, polydipsia, polyuria, fatigue
- >7 mmol/L fasting glucose or >6.5% HbA1c
106
Give an overview of the pathophysiology of T1DM
Autoimmune destruction of B cells in pancreas (produce insulin), associated w other autoimmune diseases eg. thyroid disease and Addison's.
107
What is LADA syndrome?
Latent autoimmune diabetes in adults = insidious presentation of T1Dm
108
Give an overview of the pathophysiology of T2DM
Insulin resistance due to hyperglycaemia = B cells increase insulin production but eventually give up and there is decreased B cell function.
109
What are some of the other types of diabetes?
- Pancreatic related = T3DM eg. chronic pancreatitis
- Drugs
- Endocrine causes - Cushing's, acromegaly
- MODI - monogenic cause
- Gestational causes
110
What are the drugs used in the treatment of T2DM?
- Metformin, reduces hepatic glucose production, don't use if CKD <30ml/min
- SU, increase B cell insulin release, cause weight gain and hypoglycaemia
- GLP agonists, increases insulin and satiety = weight loss and DPP-4 inhibitors stop breakdown of incretin which increases insulin, weight neutral
- Anti obesity drugs = orlastat
- SGLT-2 inhibitors, inhibits reabsorption of glucose at PCT
111
What are the complications of diabetes?
- Acute = hypoglycaemia, DKA, HHS
- Chronic = microvascular = nephropathy, neuropathy, retinopathy, macrovascular = cerebrovascular, peripheral vascular, cardiovascular eg. Charcot's foot
112
What are the complications of DKA and HHS?
```
DKA:
- Cerebral oedema
- Electrolyte disturbances = hypokalaemia
HHS:
- Arterial thrombosis
- Cerebral oedema
```
113
How do you calculate osmolality?
2Na + glucose + urea
114
What are the symptoms of hypoglycaemia?
<4mmol/L
- Sweating, palpitations, shaking, hunger
- Confusion, drowsiness, odd behaviour, speech difficulty, incoord
- Headache, nausea
115
What are the clinical features of Cushing's syndrome?
- Central obesity, dorso cervical fat pad, rounded face
- Plethera (red face)
- HTN, DM, osteoporosis
- Thin skin and easy bruising
- Proximal myopathy
116
What are the Ix into Cushing's?
- Low dose dexamethasone suppression test and overnight dexamethasone suppression test = if don't suppress cortisol = Cushing's
- 24 hr urine cortisol = elevated is Cushing's
- Need to rule out alcoholism and depression = pseudo Cushing's
117
What is the difference between Cushing's syndrome and disease?
Cushing's syndrome = any cause of excess cortisol, from outside or inside the body
Cushing's disease = specific type of Cushing's syndrome caused by ACTH producing pit adenoma
118
What are the different causes of Cushing's syndrome?
- Pit adenoma = ACTH normal or high, +ve for tumour on pit MRI
- Adrenal ACTH secreting tumour = ACTH low, hirsuitism
- Ectopic ACTH, a paraneoplastic syndrome from cancer, normally lung
119
What signs are suggestive of ectopic ACTH?
- Hypokalaemia
- History of smoking
- Weight loss
120
What is the management of each cause of Cushing's syndrome?
- Pit = trans sphenoidal removal of the pit gland
- Adrenal = lapro adrenelectomy
- Ectopic ACTH = treat underlying malignancy + medical management of cortisol if needed
121
What drugs are used for the medical control of cortisol levels?
- Metyrapone = inhibits cortisol
| - Ketoconazole = prevents ACTH secretion
122
What are the early signs of hyponatraemia?
Drowsiness, confusion and agitation
123
What are the consequences of acute severe hyponatraemia and how is it managed?
Seizures, resp depression, coma, death.
| Have to give hypertonic saline solution to avoid cerebral oedema but it is a senior decision.
124
What are the ix into hyponatraemia?
- Urine and serum osmolality
- Urine Na
- TFTs
- 9am cortisol (ACTH def + Addison's can cause)
- Drug hx important as thiazide like diuretics can cause
125
What are some of the causes of hyponatraemia? Characterise by fluid status
Hypovolaemic - burns, sweat, V+D, Addison's
Euvolaemic - SIADH, hypothyroidism
Hypervolaemic - renal, heart, liver fail, nephrotic syndrome
126
What is SIADH and what are the causes?
Syndrome of inappropriate ADH = too much water reabsorbed.
Causes = lung malignancy and can be other malignancies, anticonvulsants
Need to exclude ACTH def as it looks exactly the same by causing excess vasopressin secretion.
127
What is the management of hyponatraemia?
- Hypovolaemic hyponatraemia = normal saline
- Hypervolaemic hyponatraemia = treat underlying cause
- SIADH = reverse the cause, fluid restriction, ADH antagonists
128
What is diabetes insipidus?
Producing large volumes of dilute urine w an excessive thirst. Increased serum osmolality and reduced urine osmolality
If severe = hypernatraemia, dehydration and death.
129
Cranial DI vs nephrogenic DI
Cranial - ADH def, pit disease
| Nephrogenic DI - ADH resistance, caused by metabolic or electrolyte disturbances, can be caused by lithium
130
What can masquerade as DI?
Primary polydipsia = excessive thirst and drinking causes polyuria
131
What are the Ix into DI?
- Urine vol >3L over 24 hrs = DI
- Water deprivation test = unacceptable thirst and lose weight due to water loss indicates DI, then give synthetic ADH and urine vol decreased (cranial DI, no effect in nephrogenic)
132
How do you manage cranial DI?
Give synthetic vasopressin = desmopressin, can be administered orally, nasally, parentrally and sublingually.
133
How can you tell if you have under treated or over treated DI?
Over treated = dilutional hyponatraemia, headache and reduced cognition
Under treated = excess thirst and polyuria
134
How do you manage nephrogenic DI?
- Treat any underlying cause
- If still SE = pt should drink according to thirst to recover water loss
- Low salt, low protein diet can help
135
What are the causes of hypercalcaemia w decreased PTH?
- Malignancy, SCC secretes PTHrP and causes hypercalcaemia
| - Can also be caused by granulomatas eg. TB and sarcoidosis
136
What are the causes of hypercalcaemia w normal PTH?
Primary hyperparathyroidism until proven otherwise, usually caused by a single pit adenoma. If there is pit hyperplasia in >1 gland then normally genetic eg. MEN
137
What are the clinical features of hypercalcaemia?
- Normally found incidentally as often asymptomatic
- Vague sx = tiredness, generalised aches and pains
- Specific sx = constipation, abdo pains, kidney stones, polyuria and polydispisa due to nephrogenic DI (hypercalcaemia can cause but don't know why)
138
What is FHH?
Familial hypocalciuric hypercalcaemia = reduced Ca:creatinine ratio w normally a FH of hypercalcaemia due to defect in Ca sensory receptor
139
How can you treat hyperparathyroidism medically?
Calcimimetic drugs eg. cinacalcet that lowers Ca
140
What are the causes of hypocalcaemia?
- Post surgical hypo PTH after thyroidectomy
- Vit D def, reduced Ca and phosphate, increased PTH
- Hypomagnesaemia, func hypoPTH w normal/low PTH due to alcohol and drugs esp PPI
141
What are the clinical features of hypocalcaemia?
- Acute severe = laryngospasm, prolonged QT interval, seizures
- Muscle cramps and carpo pedal spasm
- Periorbital and peripheral paraesthesia
- Neuropsych sx
142
What is the treatment of hypocalcaemia?
- Treat underlying cause
- Acute = IV Ca
- Vit D = cholecalciferol
- HypoPTH = calcitrol and oral Ca2 supplements
- Mg def = acute IV Mg or check why there is GI loss
143
What are the triad of conditions in MEN-1?
- Pancreatic tumours
- Parathyroid hyperplasia
- Pit tumours
144
What is the treatment of hypoglycaemia?
- A to E approach
- IM glucagon or 75ml 20% glucose over 15 minutes
- Stop insulin and don't restart until BM >4mmol/ml
145
What are the causes of hypoglycaemia in a diabetic?
- Not eating enough carbs/increased exercise without carb adjustment
- Illness/stress
- Excessive alcohol consumption
- Overuse of insulin
146
What are the causes of hypoglycaemia in a non diabetic?
- Alcoholism
- Pancreatic insufficiency eg. CF or pancreatic tumour
- Anorexia/skipping meals
- Serious illness
- Adrenal pit disorder
- Hepatitis
147
What is the treatment of unbalanced Na?
Hypernatraemia - dextrose or 0.45% saline, hypotonic
| Hyponatraemia - normal saline 0.9%, hypertonic
